Factors determining the size frequency distribution of beta-amyloid (A beta) deposits in Alzheimer's disease

被引:6
|
作者
Armstrong, RA
Myers, D
Smith, CUM
机构
[1] Vision Sciences, Aston University
关键词
D O I
10.1006/exnr.1997.6465
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The size frequency distributions of discrete -amyloid (A1P) deposits were studied in single sections of the temporal lobe from patients with Alzheimer's disease. The size distributions were unimodal and positively skewed. In 18/25 (72%) tissues examined, a log normal distribution was a good fit to the data. This suggests that the abundances of deposit sizes are distributed randomly on a log scale about a mean value. Three hypotheses were proposed to account for the data: (1) sectioning in a single plane, (2) growth and disappearance of A beta deposits, and (3) the origin of A beta deposits from clusters of neuronal cell bodies. Size distributions obtained by serial reconstruction through the tissue were similar to those observed in single sections, which would not support the first hypothesis. The log normal distribution of A beta deposit size suggests a model in which the rate of growth of a deposit is proportional to its volume. However, mean deposit size and the ratio of large to small deposits were not positively correlated with patient age or disease duration. The frequency distribution of A beta deposits which were closely associated with 0, 1, 2, 3, or more neuronal cell bodies deviated significantly from a log normal distribution, which would not support the neuronal origin hypothesis. On the basis of the present data, growth and resolution of A beta deposits would appear to be the most likely explanation for the log normal size distributions. (C) 1997 Academic Press.
引用
收藏
页码:574 / 579
页数:6
相关论文
共 50 条
  • [32] Alzheimer's Disease: SPECT and PET Tracers for Beta-Amyloid Imaging
    Valotassiou, V.
    Archimandritis, S.
    Sifakis, N.
    Papatriantafyllou, J.
    Georgoulias, P.
    CURRENT ALZHEIMER RESEARCH, 2010, 7 (06) : 477 - 486
  • [33] Contribution of Beta-amyloid Accumulation to Cerebral Hypoperfusion in Alzheimer's Disease
    Fang, Xing
    Zhang, Huawei
    Border, Jane J.
    Rivers, Patrice L.
    Strong, Luke B.
    Cooper, Jonita
    Crumpler, Reece F.
    Thomas, Kirby N.
    Roman, Richard J.
    Fan, Fan
    FASEB JOURNAL, 2022, 36
  • [34] Modulation of fibrin assembly and polymerization by the beta-amyloid of Alzheimer's disease
    Merkle, DL
    Cheng, CH
    Castellino, FJ
    Chibber, BAK
    BLOOD COAGULATION & FIBRINOLYSIS, 1996, 7 (06) : 650 - 658
  • [35] Beta-amyloid auto-antibodies are reduced in Alzheimer's disease
    Qu, Bao-Xi
    Gong, Yunhua
    Moore, Carol
    Fu, Min
    German, Dwight C.
    Chang, Ling-Yu
    Rosenberg, Roger
    Diaz-Arrastia, Ramon
    JOURNAL OF NEUROIMMUNOLOGY, 2014, 274 (1-2) : 168 - 173
  • [36] Interactions between beta-amyloid and acetylcholine in the development of Alzheimer's disease
    Ehrenstein, G
    Galdicki, Z
    Lange, GD
    BIOPHYSICAL JOURNAL, 1999, 76 (01) : A54 - A54
  • [37] Inflammation and beta-amyloid in normal aging and Alzheimer disease
    d'Abramo, C
    Pronzato, MA
    Tabaton, M
    Zingg, JM
    Marinari, UM
    Ricciarelli, R
    FREE RADICAL BIOLOGY AND MEDICINE, 2004, 36 : S11 - S11
  • [38] COMPLEMENT ACTIVATION BY BETA-AMYLOID IN ALZHEIMER-DISEASE
    ROGERS, J
    COOPER, NR
    WEBSTER, S
    SCHULTZ, J
    MCGEER, PL
    STYREN, SD
    CIVIN, WH
    BRACHOVA, L
    BRADT, B
    WARD, P
    LIEBERBURG, I
    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (21) : 10016 - 10020
  • [39] PATHOLOGICAL IMPLICATIONS OF BETA-AMYLOID IN ALZHEIMER-DISEASE
    ROHER, A
    BALL, M
    JOURNAL OF NEUROCHEMISTRY, 1994, 62 : S31 - S31
  • [40] Cerebral amyloid angiopathy: A failure to eliminate beta-amyloid in Alzheimer's disease.
    Preston, S
    Wilkinson, A
    Weller, RO
    BRAIN PATHOLOGY, 2000, 10 (04) : 617 - 618